27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The systematic review and NMA includes 493 168 participants from 869 trials (adding 53 trials since October 2022) reporting data for 13 drug classes (63 drugs) and 26 outcomes of interest. 5 key findings →
Design: systematic review Participants: 168 Evidence: high
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, the spread of aberrantly phosphorylated tau is an important criterion in the Braak staging of disease severity and correlates with disease symptomatology. 4 key findings →
Participants: 654 Evidence: high
Full summary, score breakdown and related studies → Original source
Our analysis encompassed 22 RCTs involving 138,282 participants (mean age 64.8 years, 36.4% female). 5 key findings →
Design: meta-analysis Participants: 138,282 Evidence: high
Full summary, score breakdown and related studies → Original source
Targeting of tau pathology has long been proposed as a potential therapeutic strategy for Alzheimer's disease (AD). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
In a large international cardiovascular outcome trial in people with type 2 diabetes and cardiorenal disease, linagliptin did not modulate cognitive decline over 2.5 years. 2 key findings →
Participants: 1,545 Evidence: high
Full summary, score breakdown and related studies → Original source
GLP-1 RA therapy did not alter amyloid-β and tau biomarkers nor show improvements in cognition but showed potential metabolic and neuroprotective benefits. 1 key finding →
Design: systematic review Participants: 1,444 Evidence: high
Full summary, score breakdown and related studies → Original source
Fifty-eight of 77 patients (75.3%) completed the trial. 5 key findings →
Participants: 77 Evidence: high
Full summary, score breakdown and related studies → Original source
The prespecified primary analyses did not show any treatment benefit at either of the doses tested for the coprimary outcomes (change in ADAS-Cog score compared with control [n=354, 6·32, 95% CI 5·31-7·34]: 75 mg LMTM twice a day [n=257] -0·02, -1·60 to 1·56, p=0·9834, 125 mg LMTM twice a day [n=250] -0·43, -2·06 to 1·20, p=0·9323; change in ADCS-ADL score compared with control [-8·22, 95% CI -9·63 to -6·82]: 75 mg LMTM twice a day -0·93, -3·12 to 1·26, p=0·8659; 125 mg LMTM twice a day -0·34, -2·61 to 1·93, p=0·9479). 3 key findings →
Participants: 354 Evidence: high
Full summary, score breakdown and related studies → Original source
Newer GLDs were associated with a decreased risk of all-cause dementia in people with T2D. Because of the observational nature and significant heterogeneity between studies, the results should be interpreted with caution. 5 key findings →
Design: meta-analysis Participants: 819,511 Evidence: high
Full summary, score breakdown and related studies → Original source
We developed an endophenotype disease module-based methodology for Alzheimer's disease (AD) drug repurposing and identified sildenafil as a potential disease risk modifier. 2 key findings →
Design: case-control study Evidence: high
Full summary, score breakdown and related studies → Original source
From 10,037 records, 82 studies were included. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Metformin, thiazolidinediones, pioglitazone, GLP1RAs and SGLT2is were associated with reduced risk of dementia. 5 key findings →
Design: meta-analysis Participants: 100 Evidence: high
Full summary, score breakdown and related studies → Original source
Diuretic, ARB, and ACE-I use was, in addition to and/or independently of mean systolic blood pressure, associated with reduced risk of AD dementia in participants with normal cognition, while only diuretic use was associated with reduced risk in participants with MCI. 5 key findings →
Design: longitudinal study Participants: 1,928 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Each matched cohort included 23,386 (semaglutide vs sitagliptin), 22,584 (vs empagliflozin), and 19,206 (vs glipizide) patients. 5 key findings →
Design: cohort study Participants: 23,386 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Emerging evidence suggests that treatment with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) could be an interesting treatment strategy to reduce neurological complications such as stroke, cognitive impairment, and peripheral neuropathy. 3 key findings →
Design: systematic review Participants: 19 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of seven studies were included. The forest plot results showed that taking lithium therapy reduced the risk of AD (RR 0.59, 95% confidence interval [CI]: 0.44-0.78) and is also protective in reducing the risk of dementia (RR 0.66, 95% CI: 0.56-0.77). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
There are fewer than normal glucose transporters at the blood-brain barrier (BBB) in Alzheimer's disease (AD). 2 key findings →
Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source
This study (registered with PROSPERO, CRD42018085967) compares the efficacy (i.e. pro-cognitive effects) and acceptability of antidiabetic agents for Alzheimer's disease (AD) and mild cognitive impairment (MCI). 3 key findings →
Design: meta-analysis Participants: 4,855 Evidence: high
Full summary, score breakdown and related studies → Original source
In a randomized, placebo-controlled, double-blind study, we investigated whether statins alter cholesterol metabolites and reduce Abeta levels in the cerebrospinal fluid of 44 patients with Alzheimer's disease. 2 key findings →
Participants: 44 Evidence: high
Full summary, score breakdown and related studies → Original source
Statin therapy was not associated with cognitive impairment in RCTs. 5 key findings →
Design: meta-analysis Participants: 46,836 Evidence: high
Full summary, score breakdown and related studies → Original source
Participants in the placebo group displayed cognitive and functional decline, whereas lithium-treated patients remained stable over 2 years. 4 key findings →
Participants: 61 Evidence: high
Full summary, score breakdown and related studies → Original source
Treatment with GLP-1 RAs may provide a new opportunity to reduce the incidence of dementia in patients with type 2 diabetes. 2 key findings →
Participants: 15,820 Evidence: high
Full summary, score breakdown and related studies → Original source
This study provides evidence that the effects of GLP-1 receptor agonists may extend beyond their known metabolic and cardioprotective benefits to include neuroprotection, associated with a decreased risk of developing various neurodegenerative disorders. 5 key findings →
Design: cohort study Participants: 102,935 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared to the control group of patients, patients previously exposed to exenatide had an advantage of 5.6 points (95% CI, 2.2-9.0; p = 0.002) using blinded video rating of the MDS-UPDRS part 3 motor subscale. 1 key finding →
Design: randomized controlled trial Participants: 20 Evidence: high
Full summary, score breakdown and related studies → Original source
We aimed to summarise current evidence on different antidiabetic drugs to delay cognitive impairment, including mild cognitive impairment, dementia, Alzheimer's disease (AD) and vascular dementia, among subjects with type 2 diabetes mellitus (T2DM). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →